We have found that some years after apparent recovery from acute poststreptococcal glomerulonephritis (PSGN), features of continuing disease are demonstrable as manifested by glomerular sclerosis, reductions in filtration rate, and exaggerated natriuresis in response to saline loading. The major objective of our study is to achieve a better understanding of the mechanism responsible for hypertension as it occurs in the course of chronic renal disease by a prospective study of these patients following PSGN, many of whom can be expected to become hypertensive. Our approach will consist of serial studies comparing normotensive and hypertensive patients following PSGN in regard to reduction in filtering bed, the nature and extent of glomerular and vascular changes histologically, their renal and systemic responses to acute and chronic salt loading, distribution of cortical and medullary blood flow, and the presence of suppressed plasma renin activity as related to sodium homeostasis. A secondary objective is to evaluate the contribution of cellular immunity in the pathogenesis of chronicity in PSGN and other glomerular diseases, by examining lymphocytes for evidence of cellular hypersensitivity directed toward antigenic components of renal parenchyma. Parallel studies concerning the mechanism of hypertension and the pathogenesis of chronicity will be conducted in an experimental model of glomerulonephritis in the dog. BIBLIOGRAPHIC REFERENCEES: Baldwin, D.S., and Schacht, R.G.: Late Sequelae of poststreptococcal glomerulonephritis. In: Annual Review of Medicine, Vol. 27, 1975; Baldwin, D.S., and Gallo, G.R.: Lupus nephritis. In: Clinics in Rheumatic Diseases. Vol. 1, Np.3, 1975.